The role of activated acetate intermediates in the control of Escherichia coli biofilm amounts.

Abstract

A previous study postulated that acetate metabolism was a metabolic sensory mechanism that related information about E. coli's environment to the formation of biofilms (Prüβ et al., Arch. Microbiol. 2010). Considering that mutants in pta ackA (no acetyl phosphate) and ackA (high acetyl phosphate) exhibited similarly increased biofilm amounts and three dimensional structures, the hypothesis for this study was that acetyl Co-A was a more likely mediator of the acetate effect than acetyl phosphate. The effect of acetate metabolism on biofilm amounts was detailed by using single carbon sources rather than the previously used mixed amino acid medium, as well as mutations in additional genes that contribute to acetate metabolism (ldhA, pflA, pflB). In summary, the mutations in ackA, pta ackA, and ldhA increased biofilm amounts in the presence of maltose, D-trehalose, D-mannose, and L-rhamnose, all of which get converted to acetyl-CoA. The ackA mutant also exhibited increased biofilm amounts in the presence of inosine and thymidine. The mutation in pflA decreased biofilm amounts in the presence of maltotriose, uridine, D-serine, and acetate. Since ackA, pta ackA, and ldhA mutants are expected to exhibit increased intracellular acetyl-CoA levels, and pflA and pflB mutants likely exhibit decreased acetyl-CoA concentrations, we believe that acetyl-CoA is the activated acetate intermediate that controls biofilm amounts.